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 Blood, 1 November 2005, Vol. 106, No. 9, pp. 3055-3057.
Prepublished online as a Blood First Edition Paper on June 28, 2005; DOI 10.1182/blood-2005-02-0577.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Brief report

The effects of intrinsic pathway protease deficiencies on plasminogen-deficient mice

Qiufang Cheng, Yong Zhao, William E. Lawson, Vasiliy V. Polosukhin, Joyce E. Johnson, Timothy S. Blackwell, and David Gailani

From the Departments of Pathology, Medicine, and Cell and Developmental Biology, Vanderbilt University, Nashville, TN.

Plasminogen (Plg)–deficient mice experience wasting and have decreased longevity due to disseminated fibrin deposition. We generated mice with combined deficiencies of Plg and coagulation factor IX (fIX) or XI (fXI) to determine the effects on the Plg null phenotype. Mice lacking Plg and fIX (Plg–/–/fIX–/–) have lower mortality at age 6 months than Plg–/–/fIX+/+ mice (15% and 67%, respectively) and less severe wasting, consistent with the importance of fIX in fibrin formation. In contrast, combined Plg and fXI deficiency (Plg–/–/fXI–/–) reduces life span (more than 90% mortality at 6 months) and is associated with leukocyte infiltration of the lungs and pulmonary fibrosis. These abnormalities are not seen in Plg–/– or Plg–/–/fIX–/– animals. Activated fXI is thought to function primarily as a fIX activator; however, our observation suggests that fXI may have functions in regulation of inflammation or tissue repair distinct from its role in coagulation.


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